ArticleOncogene2021
Overexpression of Hmga2 activates Igf2bp2 and remodels transcriptional program of Tet2-deficient stem cells in myeloid transformation.
Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 23 citations in OpenAlex.
- Regulation of HSC development and function by Lin28b.Frontiers in cell and developmental biology · 2025Review
- Non-genotoxic carcinogens (TPA and mezerein) activate tumourous transformation through miR let-7-mediated Hmga2 expression in Bhas42 cells.Environmental epigenetics · 2025Article
- The Proteasome-Family-Members-Based Prognostic Model Improves the Risk Classification for Adult Acute Myeloid Leukemia.Biomedicines · 2024Article
- Auto-expansion ofMolecular therapy. Methods & clinical development · 2024Article
- Chromatin modifier Hmga2 promotes adult hematopoietic stem cell function and blood regeneration in stress conditions.The EMBO journal · 2024Article
- Blockade of the deubiquitinating enzyme USP48 degrades oncogenic HMGA2 and inhibits colorectal cancer invasion and metastasis.Acta pharmaceutica Sinica. B · 2024Article
- Cellular carcinogenesis in preleukemic conditions:drivers and defenses.Fukushima journal of medical science · 2024Review
- HMGA2 promotes cancer metastasis by regulating epithelial-mesenchymal transition.Frontiers in oncology · 2024Review
- Aberrant stem cell and developmental programs in pediatric leukemia.Frontiers in cell and developmental biology · 2024Review
- Article
- C2orf48 promotes the progression of nasopharyngeal carcinoma by regulating high mobility group AT-hook 2.Medical oncology (Northwood, London, England) · 2023Article
- Article
- IGF2BP2 promotes lncRNA DANCR stability mediated glycolysis and affects the progression of FLT3-ITD + acute myeloid leukemia.Apoptosis : an international journal on programmed cell death · 2023Article
- Proteomic analysis identifies HMGA2 as a novel biomarker of overall survival in papillary renal cell carcinoma.Cancer medicine · 2023Article
- Childhood hematopoietic stem cells constitute the permissive window for RUNX1-ETO leukemogenesis.International journal of hematology · 2023Review
- IGF2BP2 serves as a core m6A regulator in head and neck squamous cell carcinoma.Bioscience reports · 2022Article
- Role of TET dioxygenases in the regulation of both normal and pathological hematopoiesis.Journal of experimental & clinical cancer research : CR · 2022Review
- The acidic domain of Hmga2 and the domain's linker region are critical for driving self-renewal of hematopoietic stem cell.International journal of hematology · 2022Article
- Integrated Molecular Characterization of Patient-Derived Models Reveals Therapeutic Strategies for Treating CIC-DUX4 Sarcoma.Cancer research · 2022Article
- HMGA2 facilitates colorectal cancer progression via STAT3-mediated tumor-associated macrophage recruitment.Theranostics · 2022Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High Mobility Group AT-hook 2 (HMGA2) is a chromatin modifier and its overexpression has been found in patients with myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). Level of Hmga2 expression is fine-tuned by Lin28b-Let-7 axis and Polycomb Repressive Complex 2, in which deletion of Ezh2 leads to activation of Hmga2 expression in hematopoietic stem cells. To elucidate the mechanisms by which the overexpression of HMGA2 helps transformation of stem cells harboring a driver mutation of TET2, we generated an Hmga2-expressing Tet2-deficient mouse model showing the progressive phenotypes of MDS and AML. The overexpression of Hmga2 remodeled the transcriptional program of Tet2-deficient stem and progenitor cells, leading to the impaired differentiation of myeloid cells. Furthermore, Hmga2 was bound to a proximal region of Igf2bp2 oncogene, and activated its transcription, leading to enhancing self-renewal of Tet2-deficient stem cells that was suppressed by inhibition of the DNA binding of Hmga2. These combinatory effects on the transcriptional program and cellular function were not redundant to those in Tet2-deficient cells. The present results elucidate that Hmga2 targets key oncogenic pathways during the transformation and highlight the Hmga2-Igf2bp2 axis as a potential target for therapeutic intervention.
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